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Differential expression of prolactin receptor (PRLR) in normal and tumorous adrenal tissues: separation of cellular endocrine compartments by laser capture microdissection (LCM).

PRL stimulates adrenal steroidogenesis. In this study, we compared the PRLR expression in normal and tumorous adrenal tissues and investigated a potential proliferative effect of PRL in adrenal cells. mRNA expression of long and intermediate forms of PRLR was detected in both normal adrenal cortex as well as benign and malignant adrenal tumors and in the human adrenocortical carcinoma cell line NCI-H295. Molecular analysis of cells procured by LCM clearly demonstrated that PRLR mRNA is expressed in the adrenal cortex but not in the medulla. Immunostaining revealed PRLR protein in all three zones of the normal adrenal cortex. Furthermore, adrenal carcinomas and adenomas stained positive for the PRLR, while in phaeochromocytomas as in the normal adrenal medulla, no specific staining was observed. By WST-1 test, we could show that PRL (10(-7) M) decreased proliferation and viability of adrenal cells in primary cell culture suggesting that PRL is not a mitogenic factor of adrenocortical cells.

Adrenal Cortex↗
PubMed1989

Alpha 2-adrenoceptor stimulation inhibits cellular cyclic AMP production in microdissected human glomeruli.

The physiological role of numerically predominant alpha 2-adrenoceptor in the kidney is still unknown. This study examined the effect of alpha 2-adrenoceptor stimulation on the production of cAMP from isolated human glomeruli. Unaffected portions of human kidneys which had been removed because of renal cell carcinoma were used for the study. Glomeruli were dissected manually under a stereo microscope. In these glomeruli, alpha 2-adrenoceptor stimulation with epinephrine in the presence of propranolol inhibited significantly parathyroid hormone-dependent increases in cAMP production. This inhibitory effect of epinephrine was removed by adding a specific alpha 2-adrenoceptor antagonist, yohimbine, indicating that the inhibitory effect of epinephrine on cAMP formation was due to alpha 2-adrenoceptor stimulation. Thus, alpha 2-adrenoceptors are involved in the inhibition of cAMP production in human glomeruli.

Cyclic AMP↗